Kaur P, Ahlenius S
Department of Biochemical and Behavioral Pharmacology, Astra Arcus AB, Södertälje, Sweden.
J Neural Transm (Vienna). 1997;104(6-7):605-14. doi: 10.1007/BF01291879.
The present experiments were undertaken in order to examine mechanisms of action for reported interactions between the beta-blocker (-)-pindolol and serotonergic agents. It was found that pretreatment with (-)-pindolol (2 mg kg-1 s.c.) potentiated the stereotyped forward locomotion induced by the 5-HT2A/C receptor agonist DOI (0.125-1.0 mg kg-1 s.c.) in rats observed in an open-field arena. This (-)-pindolol/DOI-induced stereotyped forward locomotion was fully antagonized by the 5-HT2A/C receptor antagonist ritanserin (2 mg kg-1 s.c.), suggesting that (-)-pindolol enhances serotonin release, resulting i.a. in postsynaptic 5-HT2A/C receptor activation. This effect by (-)-pindolol is in all probability indirect since this compound lacks affinity for 5-HT2A/C receptors, and could be explained by reported antagonism of inhibitory serotonergic somato-dendritic 5-HT1A autoreceptors, although other possibilities related to 5-HT1B receptors or beta-adrenoceptors can not be excluded at this time. Furthermore, (-)-pindolol treatment also enhanced 5-HTP-induced (12.5-100 mg kg-1 i.p.) effects on spontaneous motor activity. These effects, however, were of smaller magnitude, and less consistent than those seen in combination with DOI.
进行本实验是为了研究β受体阻滞剂(-)-吲哚洛尔与5-羟色胺能药物之间已报道的相互作用的作用机制。研究发现,用(-)-吲哚洛尔(2mg/kg皮下注射)预处理可增强5-HT2A/C受体激动剂DOI(0.125-1.0mg/kg皮下注射)在旷场实验中诱导的大鼠刻板向前运动。这种(-)-吲哚洛尔/DOI诱导的刻板向前运动被5-HT2A/C受体拮抗剂利坦色林(2mg/kg皮下注射)完全拮抗,提示(-)-吲哚洛尔增强5-羟色胺释放,进而导致突触后5-HT2A/C受体激活。(-)-吲哚洛尔的这种作用很可能是间接的,因为该化合物对5-HT2A/C受体缺乏亲和力,这可以用已报道的抑制性5-羟色胺能体树突5-HT1A自身受体的拮抗作用来解释,尽管目前不能排除与5-HT1B受体或β肾上腺素能受体相关的其他可能性。此外,(-)-吲哚洛尔处理还增强了5-羟色氨酸(12.5-100mg/kg腹腔注射)对自发运动活动的影响。然而,这些作用的程度较小,且不如与DOI联合时一致。